ArticleEvidence-based complementary and alternative medicine : eCAM2014
Ginsenoside rb1 protects neonatal rat cardiomyocytes from hypoxia/ischemia induced apoptosis and inhibits activation of the mitochondrial apoptotic pathway.
Article in Evidence-based complementary and alternative medicine : eCAM, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- Ginsenoside Rb1 affects mitochondrial CaMolecular medicine (Cambridge, Mass.) · 2024Article
- Mitochondrial dysfunction in heart diseases: Potential therapeutic effects ofFrontiers in pharmacology · 2023Review
- Insulin-like growth factor binding protein-1 regulates HIF-1α degradation to inhibit apoptosis in hypoxic cardiomyocytes.Cell death discovery · 2021Article
- Proteomic analysis reveals ginsenoside Rb1 attenuates myocardial ischemia/reperfusion injury through inhibiting ROS production from mitochondrial complex I.Theranostics · 2021Article
- Matteucinol, isolated from Miconia chamissois, induces apoptosis in human glioblastoma lines via the intrinsic pathway and inhibits angiogenesis and tumor growth in vivo.Investigational new drugs · 2020Article
- Hormesis and Ginseng: Ginseng Mixtures and Individual Constituents Commonly Display Hormesis Dose Responses, Especially for Neuroprotective Effects.Molecules (Basel, Switzerland) · 2020Review
- Regulation of Mitochondrial Quality Control by Natural Drugs in the Treatment of Cardiovascular Diseases: Potential and Advantages.Frontiers in cell and developmental biology · 2020Review
- Effect of sulphoraphane on newborn mouse cardiomyocytes undergoing ischaemia/reperfusion injury.Pharmaceutical biology · 2019Article
- Ginsenoside Rb1 protects cardiomyocytes from oxygen-glucose deprivation injuries by targeting microRNA-21.Experimental and therapeutic medicine · 2019Article
- Estrogen receptor-β of microglia underlies sexual differentiation of neuronal protection via ginsenosides in mice brain.CNS neuroscience & therapeutics · 2018Article
- Exogenous spermine inhibits hypoxia/ischemia-induced myocardial apoptosis via regulation of mitochondrial permeability transition pore and associated pathways.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- Gensenoside Rb1 protects rat PC12 cells from oxidative stress-induced endoplasmic reticulum stress: the involvement of thioredoxin-1.Molecular and cellular biochemistry · 2015Article
- Anticancer Effect of Ursodeoxycholic Acid in Human Oral Squamous Carcinoma HSC-3 Cells through the Caspases.Nutrients · 2015Article
- Proteomic Analysis of Anticancer TCMs Targeted at Mitochondria.Evidence-based complementary and alternative medicine : eCAM · 2015Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aim. To investigate the effect of Ginsenoside Rb1 (GS-Rb1) on hypoxia/ischemia (H/I) injury in cardiomyocytes in vitro and the mitochondrial apoptotic pathway mediated mechanism. Methods. Neonatal rat cardiomyocytes (NRCMs) for the H/I groups were kept in DMEM without glucose and serum, and were placed into a hypoxic jar for 24 h. GS-Rb1 at concentrations from 2.5 to 40 µM was given during hypoxic period for 24 h. NRCMs injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. Cell apoptosis, ROS accumulation, and mitochondrial membrane potential (MMP) were assessed by flow cytometry. Cytosolic translocation of mitochondrial cytochrome c and Bcl-2 family proteins were determined by Western blot. Caspase-3 and caspase-9 activities were determined by the assay kit. Results. GS-Rb1 significantly reduced cell death and LDH leakage induced by H/I. It also reduced H/I induced NRCMs apoptosis induced by H/I, in accordance with a minimal reactive oxygen species (ROS) burst. Moreover, GS-Rb1 markedly decreased the translocation of cytochrome c from the mitochondria to the cytosol, increased the Bcl-2/ Bax ratio, and preserved mitochondrial transmembrane potential (ΔΨm). Its administration also inhibited activities of caspase-9 and caspase-3. Conclusion. Administration of GS-Rb1 during H/I in vitro is involved in cardioprotection by inhibiting apoptosis, which may be due to inhibition of the mitochondrial apoptotic pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.